Chronic Erosive Synovitis can be induced experimentally in rats by systemic administration of aqueous suspensions of cell walls from certain bacteria, such as Group A streptococci and lactobacilli. Host genetic and sex-linked hormonal factors, as well as cell wall factors, influence incidence and severity of acute and chronic disease. Arthritogenic cell walls are lysozyme resistant and are rich in rhamnose. The development of arthritis in susceptible rat strains is dependent, in variable degrees, upon deposition and persistence of the cell walls in synovial tissues. Acute arthritis reflects a direct pro-inflammatory toxic effect of the cell walls at their sites of deposition. The development of chronic arthritis is dependent upon thymus-derived lymphocytes. The chronic arthritis can be suppressed by treatment with the synthetic retinoid, 4-hydroxyphenyl-retinamide, and the immunoregulatory agent, cyclosporin A. This animal model provides a powerful tool to investigate mechanisms that regulate susceptibility and resistance to chronic inflammation, as well as, mechanisms that produce tissue injury. Potential new therapeutic agents mal also be studied.